By initially suppressing nitrogen removal and later stimulating incomplete denitrification, SMX significantly enhances emissions of nitrous oxide (N₂O)—a greenhouse gas nearly 300 times more potent than carbon dioxide.
Estuaries and coastal zones play a vital role in removing excess reactive nitrogen delivered by agriculture, wastewater, and urban runoff. This removal is largely driven by denitrification, a microbial process that converts nitrate into harmless nitrogen gas. However, denitrification can also generate N₂O as an intermediate, making these sediments both nitrogen sinks and potential greenhouse gas sources. At the same time, antibiotic use has increased sharply worldwide, and residues are now routinely detected in aquatic environments, especially in estuaries that receive upstream pollution. Previous studies have shown that antibiotics can either inhibit or stimulate denitrification and N₂O emissions, depending on dose and exposure time, but the underlying microbial mechanisms have remained unclear. Addressing these uncertainties is essential for managing eutrophication, climate impacts, and ecological risks in coastal ecosystems.
A study (DOI:10.48130/biocontam-0025-0006) published in Biocontaminant on 21 November 2025 by Guoyu Yin & Ping Han’s team, East China Normal University, uncovers a direct microbial link between antibiotic degradation and denitrification, showing that bacteria capable of breaking down SMX can also influence how reactive nitrogen is transformed and released to the atmosphere.
Using a combination of controlled sediment slurry incubations, isotope tracing, molecular quantification, and multi-omics analyses, this study systematically evaluated how SMX affects antibiotic degradation, nitrogen transformation processes, and microbial ecology. First, SMX biodegradation and nitrogen fluxes were quantified using parallel ^12C- and ^13C-labeled SMX incubations combined with ^15N tracer techniques, allowing simultaneous measurement of SMX removal, denitrification rates, and N₂O emissions. Results showed that SMX concentrations declined steadily over time, with ~80% removal by day 28 and >94% removal by day 30 in both isotope treatments, while sterile controls showed minimal loss, confirming microbial biodegradation as the dominant removal pathway. Correspondingly, denitrification rates exhibited a clear time- and concentration-dependent response: SMX significantly suppressed denitrification during the early phase (days 1–14), particularly at therapeutic concentrations, but later displayed a U-shaped pattern, with low to moderate concentrations remaining inhibitory and the highest concentration (1,000 μg L⁻¹) stimulating denitrification by day 28. In contrast, N₂O emissions were consistently enhanced by SMX exposure, increasing by up to ~180%, with emissions peaking early in the incubation. Quantitative PCR targeting functional genes revealed that SMX initially reduced the abundances of key denitrification genes (nirS, nirK, nosZ), followed by partial recovery at later stages, while sulfonamide resistance genes (sul1 and sul2) increased significantly throughout the experiment. High-throughput 16S rRNA gene sequencing demonstrated pronounced SMX-driven shifts in microbial community composition and diversity, with moderate concentrations stimulating richness and high concentrations suppressing sensitive taxa such as nitrifiers and sulfate reducers. DNA stable isotope probing further identified active SMX-assimilating microorganisms, highlighting specific bacterial groups enriched in ^13C-labeled DNA and revealing altered microbial interaction networks with reduced connectivity. Functional prediction and correlation analyses linked these community and gene-level changes to disrupted nitrogen cycling pathways, showing that SMX exposure decouples denitrification from complete N₂O reduction, thereby promoting greenhouse gas emissions while reshaping microbial resistance and degradation strategies.
These findings reveal that pharmaceutical pollution alters nitrogen cycling and greenhouse gas emissions in coastal sediments. Even environmentally relevant antibiotic concentrations increased N₂O release, suggesting that widespread contamination may enhance estuarine climate forcing. Meanwhile, adaptive denitrifiers capable of degrading antibiotics help sustain nitrogen removal under chronic pollution, though with shifted by-products.
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References
DOI
10.48130/biocontam-0025-0006
Original Source URL
https://doi.org/10.48130/biocontam-0025-0006
Funding information
This work was funded by the National Key Research and Development Program of China (2023YFC3208404 and 2024YFF0808804), the National Natural Science Foundation of China (Grant Nos 42476153, 42573078, 42371064, 42030411, and 42230505), and the Fundamental Research Funds for the Central Universities.
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